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A toolbox for Matlab Simulink (trademark of Mathworks corp. etc.) was developed to simulate various models of flow in the cardiovascular system and study effects of different pathological conditions. The toolbox was based on well-known analog lumped models of blood flow in vessels, the varying elastance heart model, blood flow through vessels, shunts, and valves as well as models of oxygen exchange at lungs and tissue. The toolbox is modular providing the basic building blocks of the cardiovascular system. Parameters for the individual components may be set by the user to adapt the component to the simulated system. Several examples are shown. This modeling system is described and is also available for downloading as an open source for free use. The authors see this as the basis for wide collaboration and standardization in modeling. A web site will be available for accepting contributions from other researchers and to create a free exchange.

Hypothesis: Transmyocardial laser revascularization (TMLR) will not denervate the heart, because it does not destroy all of the afferents. This study was designed to determine if stimulation of cardiac sympathetic and vagal afferents from an area of the left ventricle treated with TMLR could evoke reflex effects, and thus whether TMLR would denervate the heart., Methods: The effect of TMLR on reflexes evoked by chemically stimulating cardiac afferents was examined in 9 dogs. Bradykinin and capsaicin were applied topically or injected into the left anterior descending coronary artery before and after TMLR and after bilateral vagotomy and sympathectomy. Aortic (AoP) and left ventricular pressures (LVP) and electrocardiography were monitored. The first derivatives of LVP (dP/dt) were calculated., Results: Topical bradykinin elicited variable hemodynamic responses. Topical capsaicin evoked pressor responses, increasing mean (+/- SEM) AoP (105+/-9 to 115+/-9 mm Hg; P<.001) and positive dP/dt (+dP/dt) (1032+/-81 to 1159+/-10 mm Hg/s; P<.01) before TMLR. Intracoronary capsaicin evoked a depressor response before TMLR. Pressor responses remained intact after TMLR with increases in mean AoP and +dP/dt (115+/-6 to 128+/-5 mm Hg and 1039+/-98 to 1136+/-100 mm Hg/s, respectively; P<.01). Depressor responses also remained intact after TMLR (91+/-10 vs 101+/-11 mm Hg [P<.02], and 865+/-104 vs 931+/-104 mm Hg/s [P<.05], respectively). Hemodynamic responses were diminished after bilateral vagotomy and abolished after bilateral sympathectomy., Conclusion: Since activation of cardiac afferent nerves and reflex responses remained intact after TMLR, but changed after vagotomy or sympathectomy, TMLR does not denervate the heart sufficiently to be the cause of improved angina after TMLR.

Objective: Common muscle fibres encircle both ventricles and the ventricles share a common septal wall. This close anatomical association suggests that regional ischaemia and structural integrity may alter systolic function in both the right and the left ventricle. To examine this possibility, we investigated the contribution of each wall to biventricular function., Methods: Isolated hearts, obtained from anaesthetised rabbits, were perfused with physiological salt solution under constant pressure. Balloons were placed in the right and left ventricles to measure isovolumetric pressure, and pressure-volume curves were obtained. In separate sets of experiments, the left ventricular free wall, right ventricular free wall, or septum was made ischaemic, incised, or injected with glutaraldehyde, respectively. Pressure-volume curves were obtained again., Results: After left ventricular free wall ischaemia (n = 11), right ventricular developed pressure decreased significantly from 27.9(SD 8.9) to 14.1(6.6) mm Hg (p < 0.05), and remained depressed when the left ventricular free wall was further damaged by glutaraldehyde. Cutting the left ventricular free wall (n = 6) decreased right ventricular developed pressure from 28.9(8.6) to 17.8(4.8) mm Hg (p < 0.05), while reapproximating the left ventricular free wall by suturing re-established right ventricular developed pressure. After right ventricular free wall ischaemia (n = 7), right ventricular developed pressure decreased from 26.8(6.6) to 24.1(5.7) mm Hg (NS) and left ventricular developed pressure was unaltered. Cutting the right ventricular free wall (n = 7) had no effect on left ventricular developed pressure. Cutting the septum (n = 7) had no obvious influence on right ventricular developed pressure, but dramatically decreased left ventricular developed pressure from 79.2(55.2) to 43.7(32.2) mm Hg (p < 0.05). Injecting glutaraldehyde into the septum (n = 7) decreased both right and left ventricular developed pressures from 22.1(8.5) to 14.0(8.8) and from 78.2(50.5) to 47.9(37.9), respectively., Conclusions: The results show that the heart should be viewed as a mechanical syncytium. The left ventricular free wall plays a critical role in right ventricular systolic function and may help to explain the right ventricular response to left ventricular ischaemia. On the other hand, in the isolated heart preparation, right ventricular free wall ischaemia has only a minimal effect on left ventricular systolic developed pressure. Altering ventricular septal function affects both right and left ventricular systolic function.

The complex relationship among myocardial contractility, preload, afterload, and coronary autoregulation was studied using both analytical and numerical methods. To study autoregulation and coronary reserve changes in response to changes in cardiac oxygen consumption and in arterial pressure generation, a new variable was introduced: myocardial resistance to oxygen flow (RO2). This variable was defined as the ratio of the coronary driving pressure to left-ventricular oxygen uptake. High values for this variable indicate small consumption relative to the generated aortic pressure. Conditions which produce the highest obtainable value for RO2 are considered as optimal. An expression relating RO2 to ventricular hemodynamic variables was developed and studied using a mathematical model of the cardiovascular system. The model included a mechanism of local autoregulation based on the assumption that, in steady state, the amount of oxygen consumed equals the amount extracted from coronary blood. Heart rate, peripheral resistance, end-diastolic volume, and myocardial contractility were varied while the coronary circulation was adjusted to meet ventricular oxygen consumption at each state. The model predicts that, for each state of the circulation, there is an optimal level of cardiac contractility for which the coronary reserve is maximized.

To examine the importance of systolic ventricular interdependence on right ventricular function, we used a unique electrically isolated right ventricular free wall preparation. Double-peaked waveforms for right ventricular pressure and pulmonary arterial blood flow occurred over a wide range of pacing intervals between the left and right ventricles. One component of the waveforms could be directly related to right ventricular free wall contraction, whereas the other component was directly related to left ventricular and septal contraction. For left ventricular pressure, the left ventricular component was significantly larger than the right ventricular free wall component (92.7 +/- 3.2 vs. 7.3 +/- 3.2% peak-to-peak value, P less than 0.01). For right ventricular pressure, the left ventricular and septal component was significantly greater than the right ventricular component (63.5 +/- 10.9 vs. 36.5 +/- 10.9% peak-to-peak value, P less than 0.05). Similarly, for pulmonary arterial blood flow, the left ventricular component was significantly greater than the right ventricular component. When right ventricular free wall pacing stopped in diastole, 68 +/- 4% of right ventricular systolic pressure and 80 +/- 4% of pulmonary flow were obtained in the subsequent beat. The results of this study indicate that left ventricular contraction is very important for right ventricular developed pressure and volume outflow.

Study Objective: The mechanical coupling between the ventricles occurs directly through the myocardium (ventricular-ventricular coupling) and indirectly through the pericardium (ventricular-pericardial-ventricular coupling). We postulated that the magnitude of ventricular-pericardial-ventricular coupling would increase at high pericardial pressures, while ventricular-ventricular coupling would be unaltered., Design: Canine hearts were removed and placed in cold cardioplegic solution. Balloons were inserted into each ventricle and the left and right ventricular pressure (dP1, dPr) and volume (dV1, dVr) changes caused by increasing the pressure and volume of the other ventricle and by increasing pericardial pressure (dPp) were measured., Experimental Materials: Hearts from 10 random source dogs, weight 12.5-18 kg, were used., Measurement and Main Results: At control pericardial pressure levels, the magnitude of the pericardial-ventricular interactions was greater than the ventricular-ventricular interactions: dP1/dPp was significantly greater than dP1/dPr, at 0.71 (SEM 0.04), n = 6, v 0.18 (0.03), p less than 0.01, and dV1/dPp was significantly greater than dV1/dPr, at -0.83 (0.09) v -0.24 (0.06), p less than 0.05. Raising the pericardial pressure increased the mechanical coupling between the ventricles: dP1/dPr approximately, dV1/dPr approximately, dPr/dP1 approximately, and dVr/dP1 approximately increased significantly (p less than 0.05) by 0.48 (0.03), 0.67 (0.13), 0.38 (0.05), and 0.61 (0.09) respectively. This increased coupling occurred through pericardial pressure changes. If pericardial pressure was maintained constant, the coupling between the ventricles was unaltered. This same pattern was observed in four in situ experiments. For these experiments, at the raised pericardial pressure levels, dP1/dPr increased, from 0.51 (0.03) to 0.79 (0.01), p less than 0.05, if pericardial pressure was allowed to vary, but was unaltered with a constant pericardial pressure, at 0.42 (0.03) v 0.44 (0.04), p greater than 0.5., Conclusions: Ventricular interdependence was increased with raised pericardial pressure and this increased coupling was due primarily to an increased ventricular-pericardial-ventricular coupling. This increased coupling may help to explain the paradoxical pulse observed in cardiac tamponade.

The effects of the pericardium on myocardial diastolic ventricular interaction during early development were determined in vitro using hearts excised from eight preterm (109 +/- 0.106 SE d gestation; term = 147 d) and eight newborn (2.3 +/- 0.30 SE d postnatal age) lambs. The lamb hearts were excised with the pericardium intact and immersed in a cold cardioplegic solution. Subsequently, very compliant balloon catheters were inserted into the right and left ventricles retrograde through the pulmonary artery and aorta respectively. Before and after the removal of the pericardium, the changes in left ventricular pressure or volume caused by increasing right ventricular pressure or volume were measured. Computerized analysis of the pressure and volume recordings yielded pressure and volume transfer functions that quantified ventricular interaction. The pressure transfer functions (left ventricular pressure/right ventricular pressure) both with and without the pericardium intact were 0.297 +/- 0.010 SE and 0.140 +/- 0.005 SE, respectively, for the preterms and 0.650 +/- 0.033 SE and 0.301 +/- 0.031 SE for the newborns. The volume transfer functions (left ventricular volume/right ventricular volume) with and without the pericardium were 0.320 +/- 0.04 SE and 0.150 +/- 0.024 SE, respectively, for the preterm and 0.514 +/- 0.052 SE and 0.233 +/- 0.027 SE for the newborns. These data demonstrate that 1) the pericardium increases ventricular interaction in both preterm and newborn lambs and 2) the relative percentage increase is similar for both age groups and not age dependent. Furthermore, these findings suggest that the increase in ventricular interaction due to the presence of the pericardium is mediated by the relative compliances of the free walls, septum, and pericardium.

We evaluated the contribution of the thorax and the undisturbed pericardium to the external pressure of the euvolemic left ventricle in thirteen anesthetized dogs. Left ventricular (LV) end-diastolic pressure (EDP) in the euvolemic state was 7 +/- 2 mmHg initially and increased to 10 +/- 2 mmHg after the chest and pericardium were opened. LV end-diastolic volume (conductance catheter) was 43 +/- 20 ml initially and did not change after the chest or the pericardium was opened. Intrathoracic (PIT) and pericardial (PPER) pressures were calculated as the difference in LV chamber pressure before and after opening these spaces. Thus for the LV, PIT was -3 +/- 1 mmHg, and PPER was 0 +/- 2 mmHg. Isovolumic relaxation, early diastolic filling, and total diastolic filling were not significantly altered after the chest or pericardium was opened. Thus under euvolemic conditions in this model pericardial pressure is negligible, and the external pressure of the undisturbed left ventricle is negative and equal to intrathoracic pressure.

We investigated left ventricular (LV) early diastolic filling in 10 normal conscious dogs that had been previously instrumented to measure LV and left atrial (LA) pressures and three orthogonal LV internal dimensions. LV volume was calculated as a general ellipsoid. The pressure within a passive structure increases as it is filled. If myocardial relaxation is rapid enough to substantially aid LV diastolic filling, it may overcome this effect and cause LV pressure to fall despite an increase in volume. Thus, we defined the amount of LV filling that occurred while LV pressure was falling as relaxation filling, which is a measure of the importance of LV relaxation during early diastolic filling. The time constant of relaxation (T) was derived from the exponential fall of LV pressure during isovolumic relaxation. While LV pressure was falling early in diastole (the relaxation filling period), all three LV diameters increased. Autonomic blockade with hexamethonium (5 mg/kg) and atropine (0.1 mg/kg) reduced relaxation filling from 21 +/- 6% (mean +/- SD) to 12 +/- 3% of the stroke volume (p less than 0.01). The mean LA pressure also was significantly decreased (from 12 +/- 2 to 10 +/- 5 mm Hg, p less than 0.05), while the duration of the relaxation filling period and T were unchanged. Positive inotropic stimulation with dobutamine (10 micrograms/kg/min) shortened T without changing LA pressure. The maximum LA-LV pressure gradient, dV/dtmax, and relaxation filling all increased. Augmented preload produced by dextran infusion (500 ml/10 min) caused an increase in LA pressure (from 11 +/- 3 to 21 +/- 8 mm Hg, p less than 0.05) without altering T. This also increased the maximum LA-LV pressure gradient, dV/dtmax, and relaxation filling. Augmented afterload produced by methoxamine (10 mg/3 min i.v.) significantly increased LA pressure (from 9 +/- 4 to 15 +/- 10 mm Hg, p less than 0.05) and lengthened T (from 35 +/- 4 to 50 +/- 7 msec, p less than 0.05) and the duration of relaxation filling (from 36 +/- 5 to 44 +/- 9 msec, p less than 0.01) without altering the maximum LA-LV pressure gradient, dV/dtmax, or LV relaxation filling. Incremental changes in heart rate induced by atrial pacing (from 100-180 beats/min) resulted in progressive decreases in the time constant of LV relaxation and the duration of relaxation filling. The LA pressure was also decreased. There was no corresponding increase in the amount of active LV filling until the heart rate reached 180 beats/min. During all these interventions, T correlated with the duration of LV relaxation filling (r = 0.99. p less than 0.05). The amount of relaxation filling and dV/dtmax both correlated with the maximum LA-LV pressure gradient.(ABSTRACT TRUNCATED AT 400 WORDS)

We evaluated catheterization laboratory data from 691 individuals (219 normals and 472 coronary patients) using a computerized data file that provided several measures of cardiovascular performance in 10-year age increments. The expected increase in arterial pressure with age was noted in normals and coronary patients. Left ventricular end diastolic pressure, end diastolic volume, and end systolic volume remained constant with age but were higher in all age groups in the coronary patients. Ejection fraction showed no change with age but was lower in all age groups in patients with coronary disease. Left ventricular mass increased with age in normals and coronary patients. Cardiac index declined with age, whereas arteriovenous oxygen difference and oxygen consumption were unchanged. Age-related changes in the circulation were for the most part unaffected by the presence of coronary disease. Resting left ventricular function was not altered by age but coronary disease produced a decline in left ventricular function in all ages.

With respiration, right ventricular end-diastolic volume fluctuates. We examined the importance of these right ventricular volume changes on left ventricular function. In six mongrel dogs, right and left ventricular volumes and pressures and esophageal pressure were simultaneously measured during normal respiration, Valsalva maneuver, and Mueller maneuver. The right and left ventricular volumes were calculated from cineradiographic positions of endocardial radiopaque markers. Increases in right ventricular volume were associated with changes in the left ventricular (LV) pressure-volume relationship. With normal respiration, right ventricular end-diastolic volume increased 2.3 +/- 0.7 ml during inspiration, LV transmural diastolic pressure was unchanged, and LV diastolic volume decreased slightly. This effect was accentuated by the Mueller maneuver; right ventricular end-diastolic volume increased 10.4 +/- 2.3 ml (P less than 0.05), while left ventricular end-diastolic pressure increased 3.6 mmHg (P less than 0.05) without a significant change in left ventricular end-diastolic volume. Conversely, with a Valsalva maneuver, right ventricular volume decreased 6.5 +/- 1.2 ml (P less than 0.05), and left ventricular end-diastolic pressure decreased 2.2 +/- 0.5 mmHg (P less than 0.05) despite an unchanged left ventricular end-diastolic volume. These changes in the left ventricular pressure-volume relationship, secondary to changes in right ventricular volumes, are probably due to ventricular interdependence. Ventricular interdependence may also be an additional factor for the decrease in left ventricular stroke volume during inspiration.

Cardiovascular effects of positive end-expiratory pressure (PEEP) at 20 cmH2O were examined in six mongrel dogs (11.3-15.0 kg). The dogs were anesthetized through a combination of intramuscular Innovar and gaseous anesthesia (60% N2O-40% O2). For volume measurements, radiodense tantalum screws were placed on the endocardial surface of the left and right ventricle. Esophageal and left and right ventricular pressures were measured. With the use of this preparation, the effects of positive end-expiratory pressure (PEEP = 20 cmH2O) on cardiovascular function were examined. PEEP caused right ventricular transmural pressures to decrease, 3.4 +/- 1.0 to 2.0 +/- 1.0 mmHg end-diastolic (P less than 0.05) and 29.2 +/- 2.2 to 27.9 + 2.2 mmHg peak systolic; left ventricular transmural pressures decreased, 5.9 +/- 1.6 to 1.2 +/- 1.4 mmHg end-diastolic (P less than 0.05) and 117.2 +/- 8.0 to 76.2 +/- 7.4 mmHg peak systolic (P less than 0.05). After volume loading the animal (500 ml dextran), PEEP caused similar changes in right and left ventricular pressures. Plots of end-diastolic volume versus pressure showed an increase in the apparent diastolic stiffness in both ventricles with decreased end-diastolic volume.

Biplane ventriculography was performed on nine intact anesthetized rats. Images of the left ventricle large enough for analysis were obtained by placing the rats close to the radiographic tubes (direct enlargement). Sampling rates, adequate for heart rates of 500 beats/min, were obtained by filming at 500 frames/s. From the digitized silhouettes of the left ventricle the following information was obtained (means +/- SE): end-diastolic volume 0.60 +/- 0.03 ml, end-systolic volume 0.22 +/- 0.02 ml, stroke volume 0.38 +/- 0.02 ml, ejection fraction 0.63 +/- 0.02, cardiac output 118 +/- 7 ml/min, diastolic septolateral dimension 0.41 +/- 0.01 mm, diastolic anteroposterior dimension 0.40 +/- 0.01 mm, diastolic base-to-apex dimension 1.58 +/- 0.04 mm. To determine the accuracy with which the volume of the ventricle could be measured, 11 methyl methacrylate casts of the left ventricle were made. The correlation was high (r = 0.99 +/- 0.02 ml E) between the cast volumes determined by water displacement and by use of two monoplane methods (Simpson's rule of integration and the area-length method applied to the analysis of the anteroposterior films) and a biplane method (area-length). These results demonstrate that it is possible to obtain accurate dimensions and volumes of the rat left ventricle by use of high-speed ventriculography.

Radiopaque markers implanted in the heart have been used both clinically and experimentally to examine cardiac function. From the position of the markers, both regional and global function can be determined. A major problem with using radiopaque markers is the excessive time required for data analysis. Each marker in every cine frame must be identified and digitized by the investigator. To circumvent this problem, a computer system was developed to automatically identify the markers. The cine film is projected onto a TV camera from which the video signal is digitized and transferred into a computer. The investigator identifies the markers in the first cine frame and thereafter the computer advances the film and locates the markers. The markers are recognized based on positional information from the previous cine frame and on a video density profile. This system greatly reduced the investigators' time required for data analysis.

Although the measurement of transmural pressure is important, calculation of transmural pressure is complicated by the difficulties in measuring pericardial pressure. Recently, flat balloons have been proposed to measure pericardial pressure. Over a wide range of volumes, right ventricular diastolic pressure and pericardial balloon pressure were similar in diastole, suggesting that the right ventricle is unstressed at physiologic volumes and that right atrial pressure can be used to estimate pericardial pressure. To evaluate these concepts and to assess indirectly the accuracy of measuring pericardial pressure using flat balloons, six canine hearts were examined postmortem. The pericardium was removed and the hearts were submerged in cold cardioplegic solution. Balloons were inserted into the right and left ventricles, and right and left ventricular pressure-volume curves were obtained. Right ventricular transmural pressures of 2.6 +/- 0.5, 3.9 +/- 0.9, 5.9 +/- 1.4, and 8.9 +/- 2.4 mm Hg were required to distend the right ventricle to 10, 20, 30, and 40 ml, respectively. For the left ventricle, transmural pressures of 3.4 +/- 0.7, 5.4 +/- 1.2, 8.6 +/- 2.1, and 14.1 +/- 3.8 mm Hg were recorded at volumes of 10, 20, 30, and 40 ml, respectively. Although the right ventricular transmural pressures were less than the left ventricular transmural pressures over the physiologic range, right ventricular transmural pressures were always positive and increased with increments in ventricular volume. Thus the right ventricle is not unstressed over the entire range of physiologic volumes, suggesting that pericardial balloon pressures may overestimate pericardial pressure and that right atrial pressure cannot be used to estimate pericardial pressure.

To better understand biventricular mechanics, an algorithm was developed to simultaneously calculate right and left ventricular volumes from randomly placed subendocardial radiopaque markers. Mathematically, the ventricle is represented as a stack of circular discs. The radius R of each disc is calculated as the distance from the subendocardial radiopaque marker to a computer generated base-to-apex line, and the height H of each disc is determined by the projected distance between radiopaque markers along the base-to-apex line. Accordingly, the volume (V) is calculated as V = pi . sigma Hi . Ri2. The validity of this algorithm was tested on 10 canine left ventricular casts, on 10 human right ventricular casts, and in five experiments. For the left ventricle, the regression line between the casts (VT) and calculated (VC) volumes was VC = 0.55 VT + 6.6, with r = 0.95, standard error of estimate (Sy) = 1.9 ml, and the standard deviation of percent error = 12.6%. For the right ventricle, VC = 1.75 VT = 42.5, with r = 0.86, Sy = 16.2 ml, and the standard deviation of percent error = 24.8%. In five animal experiments, radiopaque markers were implanted into the endocardium of the left and right ventricles and comparisons were made between angiographic- and marker-determined ventricular volumes. For the five experiments, the mean correlation coefficient, relating the marker volumes to the angiographic volumes, were 0.92 +/- 0.01 for the left ventricle and 0.89 +/- 0.02 for the right ventricle. The results, which are similar to other volume-determination methods, indicate that this method can be applied to determine right and left ventricular volume. Once implanted, fluoroscopy of these markers provides a noninvasive means of calculating ventricular volume.

Based on the balance of forces across the interventricular septum, we developed a theoretical analysis to explain how one ventricle can directly influence the filling characteristics of the other ventricle. The analysis indicated that the pressure and volume transfer were related to the relative compliances of the interventricular septum and ventricular free walls. The present study examined whether the theoretical analysis could be used to predict changes in ventricular interdependence caused by altering regional compliance. To examine this hypothesis, hearts were removed from 18 dogs and placed in cool cardioplegic solution. Balloons were inserted into each ventricle, and the left and right pressure (delta P1, delta Pr) and volume (delta V1, delta Vr) changes caused by changing the pressure and volume of the other ventricle were recorded. After the initial measurements, acute changes in left ventricular free wall compliance (n = 6), septal compliance (n = 6), and right ventricular free wall compliance (n = 6) were induced by glutaraldehyde injections. As predicted by the theoretical analysis, decreasing left ventricular free wall compliance increased delta P1/delta Pr, delta P1/delta Vr, delta Pr/delta V1, and delta Vr/delta V1 significantly (P less than 0.05) by 89 +/- 15, 155 +/- 33, 282 +/- 65, and 112 +/- 22% (mean +/- SEM), respectively. Decreasing septal compliance decreases delta P1/delta Pr, delta V1/delta Pr, delta V1/delta Vr, delta Pr/delta P1, delta Vr/delta P1, and delta Vr/delta V1 significantly (P less than 0.05) by 48 +/- 7, 71 +/- 10, 69 +/- 14, 48 +/- 7, 62 +/- 8, and 57 +/- 13%, respectively. Decreasing right ventricular free wall compliance increased delta P1/delta Vr, delta V1/delta Vr, delta Pr/delta P1, and delta Pr/delta V1 significantly (P less than 0.05) by 97 +/- 25, 79 +/- 20, 57 +/- 18, and 59 +/- 23%, respectively. Furthermore, these alterations in ventricular coupling were predictable: The actual and predicted percentage changes in the transfer functions were in close agreement. The results of these studies show predictable alterations in the mechanical coupling between the ventricles following changes in right ventricular, septal, and left ventricular free wall compliances.

Because of the close anatomic connections, the volume in 1 ventricle can directly influence the volume in the other ventricle. We examined this ventricular mechanical coupling at elevated pericardial pressures in 6 mongrel dogs. The animals were anesthetized and were mechanically ventilated with intermittent positive-pressure ventilation. Right and left ventricular volumes and pressures and pericardial pressure were simultaneously measured during control and after infusing 25, 50, and 75 ml of saline with dextran into the pericardial cavity. The ventricular volumes were calculated from cine-radiographic positions of endocardial, radiopaque markers. In the control state, right ventricular end-diastolic volume (RVEDV) increased 9.2 +/- 0.9 ml (p less than 0.05) during expiration, whereas left ventricular end-diastolic pressure (LVEDP) increased 0.6 +/- 0.7 mmHg and left ventricular end-diastolic volume (LVEDV) decreased 0.6 +/- 0.4 ml. The increased transmural LVEDP with a decreased LVEDV indicates an apparent left ventricular distensibility decrease as right ventricular diastolic volume increased, possibly because of ventricular interdependence. At the highest pericardial pressure, RVEDV increased 6.7 +/- 1.4 ml (p less than 0.05) during expiration as LVEDP increased 1.2 +/- 0.6 mm Hg and LVEDV decreased 2.0 +/- 0.6 ml (p less than 0.05). Thus, at the higher pericardial pressures, smaller changes in RVEDV produced significantly greater changes in LVEDV. This coupling between the ventricles was further examined in 5 hearts studied postmortem. The hearts were placed in cold cardioplegic solution and balloons were inserted into both ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)

The possibility that left ventricular (LV) performance might affect right ventricular (RV) function through the myocardium was examined by using isolated, flow-perfused, paced rabbit hearts beating isovolumically. Reducing LV volume from its optimal volume to zero caused a 5.7% decrease (N = 10, P less than 0.001) in right ventricular developed pressure (RVDP). Ligating the anterior ventricular branches of the left coronary artery which in the rabbit supply the LV free wall resulted in an additional 9.3% decrease in RVDP (N = 5, P = 0.05) within 3 min of ligation. Finally, cutting the LV free wall from the atrioventricular orifice to the apex (thereby preventing any developed LV free wall force during systole) caused a 45% further decrease in RVDP (N = 2, P less than 0.02). Cineradiographic study showed that the alterations in RVDP resulting from changes in LV volume and coronary occlusion correlated significantly (N = 5, P less than 0.01) with the magnitude of septal bulging into the RV cavity during systole. The results indicate that alteration in LV free wall function and changes in LV volume can directly effect RVDP through the myocardium.

Because of the close anatomical association between the ventricles, the volume of one ventricle can directly affect the volume and pressure within the other ventricle. To study the mechanical coupling between the ventricles, we modeled the right and left ventricles as a two-compartment model with right wall (Crw), septal (Cs), and left wall (Clw) compliances. Based on the balances of forces across the septum, four equations were obtained to predict the transfer of pressure (P) and volume (V) information from one ventricle to another. The validity of the theoretical analysis was tested first in a physical model and then in a post-mortem heart preparation. The standard errors of estimate comparing the predicted to measured values were low for both the physical model and the post-mortem heart data. All values were significantly related (P less than 0.05) with r greater than 0.89. The results show excellent correlation between predicted and measured values. This model provides a better understanding of ventricular interdependence and may help to predict effects of hypertrophy and/or myocardial ischemia on ventricular interdependence.

Because of ventricular interdependence, part of the measured left ventricular diastolic pressure can be attributed to the right ventricle. Therefore, we examined the hypothesis that left ventricular diastolic properties are modified by alterations in right ventricular compliance and pressure even without a change in right ventricular volume. To examine this hypothesis, the hearts were removed from six dogs, the coronary arteries perfused with cool cardioplegic solution, and the hearts submerged in cool cardioplegic solution. Balloons were inserted into each ventricle. Left ventricular pressure-volume curves were recorded and approximated by an exponential equation. With no fluid in the right ventricular balloon (control), the exponential coefficient and constant were 0.038 (SD 0.004) ml-1 and 2.38(0.75) mm Hg respectively. With right ventricular pressure held constant at 20 mm Hg, the exponential coefficient and constant were 0.035(0.002) ml-1 and 3.71(1.64) mm Hg (p less than 0.05 v control constant), respectively. With a fixed right ventricular volume, the exponential coefficient and constant were significantly different (p less than 0.05 v control values) at 0.040(0.006) ml-1 and 2.81(0.96) mm Hg, respectively. After decreasing right ventricular free wall compliance by injecting glutaraldehyde into the right coronary artery, the exponential coefficient and constant were significantly different (p less than 0.01 v control values) at 0.058(0.010) ml-1 and 1.86(0.60) mm Hg, respectively. Thus, even with a constant right ventricular pressure or volume, a significant upward shift in the left ventricular pressure-volume relation occurred. Decreasing right ventricular free wall compliance further increased left ventricular pressure. The results of these studies indicate that the diastolic properties of the left ventricle can be modified by changes in right ventricular pressure and compliance even without a change right ventricular volume. Thus indices of left ventricular diastolic properties may be altered by changes in the characteristics of the right ventricle.

The pressure and volume in one ventricle can directly influence the pressure and volume in the other ventricle. Since this mechanical coupling depends on the anatomical structure of the heart, we postulated that disease states which alter regional ventricular compliance will alter the mechanical coupling between the ventricles. We examined this hypothesis in six dogs, each with a prior myocardial infarction involving solely the left ventricular free wall. The animals were sacrificed, the hearts removed and placed in cool cardioplegic solution. Balloons were inserted into each ventricle and the left and right pressure (dPl,dPr) and volume (dVl,dVr) changes (or transfer) caused by change to the pressure and volume of the other ventricle were recorded. In five additional experiments, acute changes in compliance were induced by injecting glutaraldehyde into the left ventricular free wall. The results of these experiments were compared to four control experiments. As compared to the control experiments, the transfer functions dPl/dPr, dPl/dVr, dPr/dVl, and dVr/dVl increased significantly (p less than 0.05) in the infarct and glutaraldehyde groups, while the transfer functions dVl/dPr, dVl/dVr, dPr/dPl and dVr/dPl were unaltered in the infarct and glutaraldehyde groups. The results of these studies show significant selective alteration in the mechanical coupling between the ventricles following left ventricular free wall infarction.